Two major classes of FLT3 mutations exist in AML: (a) internal tandem duplication (ITD) in the juxtamembrane domain, detected in around 23% of AML cases, and (b) point mutations in the tyrosine kinase domain (TKD), identified in 7% of AML patients.1 Mutations also occur in other members of the class III receptor tyrosine kinase family, including c‐KIT, which can be expressed as ITDs with an overall incidence of 17%,2 and platelet‐derived growth factor receptors α and β (PDGFRA and PDGFRB), which are more rare.3, 4. This evidence concerns the gene KIT and acute myeloid leukemia.